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Annual Review of Pathology-Mechanisms of Disease最新文献

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Targeting Genome Stability to Mitigate Human Aging and Disease. 靶向基因组稳定性减缓人类衰老和疾病。
IF 36.2 1区 医学
Annual Review of Pathology-Mechanisms of Disease Pub Date : 2025-10-14 DOI: 10.1146/annurev-pathmechdis-042624-105942
Debra Toiber,Björn Schumacher
{"title":"Targeting Genome Stability to Mitigate Human Aging and Disease.","authors":"Debra Toiber,Björn Schumacher","doi":"10.1146/annurev-pathmechdis-042624-105942","DOIUrl":"https://doi.org/10.1146/annurev-pathmechdis-042624-105942","url":null,"abstract":"The maintenance of a stable genome requires constant repair. Congenital DNA repair defects lead to cancer susceptibility and progeroid (premature aging-like) syndromes. Even with intact repair, DNA lesions accumulate in aging organisms, leading to replication and transcription stress and age-dependent somatic mutations. These, in turn, can compromise cellular function and elevate cancer risk. DNA damage response (DDR) mechanisms can lead to cellular death and senescence, and targeting the DDR has emerged as therapeutic strategy not only in cancer but also to protect from age-associated phenotypes. Inhibiting DNA repair can promote cancer cell death. Eliminating senescent cells may alleviate proinflammatory consequences on their tissue environment. Moreover, strategies to limit DNA damage and augment repair in normal cells are in active development. Here, we review emerging concepts for targeting genome maintenance mechanisms to lower cancer risk and lengthen healthy lifespan by extending the integrity and functionality of somatic genomes.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"8 1","pages":""},"PeriodicalIF":36.2,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145288203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Molecular Pathogenesis of Uterine Sarcomas: Mechanisms and Implications for Treatment. 子宫肉瘤的分子发病机制及其治疗意义。
IF 36.2 1区 医学
Annual Review of Pathology-Mechanisms of Disease Pub Date : 2025-10-14 DOI: 10.1146/annurev-pathmechdis-111523-023434
Sarah Chiang
{"title":"Molecular Pathogenesis of Uterine Sarcomas: Mechanisms and Implications for Treatment.","authors":"Sarah Chiang","doi":"10.1146/annurev-pathmechdis-111523-023434","DOIUrl":"https://doi.org/10.1146/annurev-pathmechdis-111523-023434","url":null,"abstract":"Uterine sarcomas are rare cancers with diverse clinical, histologic, and genomic profiles. At the genetic level, they can be classified into simple and complex genomic sarcomas, exemplified by endometrial stromal sarcoma (ESS) and uterine leiomyosarcoma (uLMS), respectively. Sequencing technologies in research and clinical settings have significantly advanced the molecular understanding of these tumors. New entities characterized by distinctive morphologies and genomic alterations have expanded the category of uterine sarcomas with simple genomes beyond ESS to include variant uLMS and fibrosarcoma-like uterine sarcoma (FUS). Molecular profiling of uLMS has also uncovered possible therapeutic targets in the most common type of uterine sarcoma, where prognostication and clinical management remain challenging. This review discusses the current histologic and molecular classification of low- and high-grade ESS, FUS, and conventional and variant uLMS and explores the potential impact of the genetic alterations observed in these uterine sarcomas on treatment.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"13 1","pages":""},"PeriodicalIF":36.2,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145288204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Zonation, Zonation, Zonation: The Real Estate of the Liver 分区，分区，分区：肝脏的房地产
IF 36.2 1区 医学
Annual Review of Pathology-Mechanisms of Disease Pub Date : 2025-10-13 DOI: 10.1146/annurev-pathmechdis-042624-091820
Tyler M. Yasaka, Chang Kyung Kim, Vik Meadows, Satdarshan P. Monga
{"title":"Zonation, Zonation, Zonation: The Real Estate of the Liver","authors":"Tyler M. Yasaka, Chang Kyung Kim, Vik Meadows, Satdarshan P. Monga","doi":"10.1146/annurev-pathmechdis-042624-091820","DOIUrl":"https://doi.org/10.1146/annurev-pathmechdis-042624-091820","url":null,"abstract":"The liver serves as a central hub for a diverse set of functions including metabolic homeostasis, detoxification, and protein synthesis. While appearing homogeneous, hepatocytes, the major workhorse in the liver, demonstrate spatial identity within the lobule, which in turn dictates gene and protein expression and, eventually, function. Presenting as an axis from the portal triad to the central vein, this organization has been conventionally referred to as metabolic zonation. In recent years, the heterogeneity in expression and function is now understood to extend well beyond hepatocytes and metabolism to include nonparenchymal cells and diverse functions. Although the lobule is conventionally divided into three zones, spatial multi-omics technologies reveal a more nuanced picture, where zonation provides a coordinate system for an eclectic but highly functional hepatic milieu. We summarize the current understanding of liver zonation as it contributes to division of labor, injury compartmentalization, and stepwise arrangement of metabolic pathways and discuss the implications of this framework for liver homeostasis, regeneration, and disease.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"7 1","pages":""},"PeriodicalIF":36.2,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145282668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Gasdermins, Executors of Pyroptosis: A Decade in Perspective. Gasdermins，焦亡的执行者：十年的观点。
IF 36.2 1区 医学
Annual Review of Pathology-Mechanisms of Disease Pub Date : 2025-10-09 DOI: 10.1146/annurev-pathmechdis-042624-121548
Bowen Zhou,Derek Abbott
{"title":"Gasdermins, Executors of Pyroptosis: A Decade in Perspective.","authors":"Bowen Zhou,Derek Abbott","doi":"10.1146/annurev-pathmechdis-042624-121548","DOIUrl":"https://doi.org/10.1146/annurev-pathmechdis-042624-121548","url":null,"abstract":"Pyroptosis is a molecularly defined pathway of cell death and lysis relying on formation of membrane pores by the family of gasdermin proteins. Since the characterization of prototypical gasdermin D in 2015, intense effort in the past decade has shed light on protease-dependent activation of these agents of cellular demise in human health and disease, although cell death-independent functions do exist. Numerous regulatory mechanisms ranging from posttranslational modification, control of expression, and overlap in activation systems have been described, but pharmacologic control of gasdermins is still in its infancy. Thus, gasdermin-specific targeting in disease has not yet been achieved outside of a few select cases. This review summarizes these findings broadly from a perspective of biological mechanisms and highlights the forthcoming challenges hindering bench-to-bedside adoption of this knowledge.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"39 1","pages":""},"PeriodicalIF":36.2,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145254532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Immunopathology of Glioblastoma 胶质母细胞瘤的免疫病理学
IF 36.2 1区 医学
Annual Review of Pathology-Mechanisms of Disease Pub Date : 2025-10-08 DOI: 10.1146/annurev-pathmechdis-042524-025950
Jiabo Li, James L. Ross, Dolores Hambardzumyan, Daniel J. Brat
{"title":"Immunopathology of Glioblastoma","authors":"Jiabo Li, James L. Ross, Dolores Hambardzumyan, Daniel J. Brat","doi":"10.1146/annurev-pathmechdis-042524-025950","DOIUrl":"https://doi.org/10.1146/annurev-pathmechdis-042524-025950","url":null,"abstract":"Glioblastoma (GBM), the most frequent and malignant primary brain tumor, is characterized by a highly diverse and profoundly immunosuppressive tumor microenvironment (TME) that provides an unconstrained environment for tumor progression and significantly complicates therapeutic interventions. Despite advances in immunotherapeutic approaches, such as chimeric antigen receptor T cell and immune checkpoint inhibitors, efficacy remains limited due to the complexity of the GBM TME and robust immune evasion mechanisms. In this review, we elucidate the intricate interplay among cellular components within the TME that lead to this immunosuppressive state, including tumor-associated macrophages/microglia, myeloid-derived suppressor cells, regulatory T cells, and glioma stem cells, as well as other critical elements that contribute to TME complexity, such as the severe hypoxia associated with central necrosis, the blood–brain barrier, and the extracellular matrix. This review also highlights mechanisms of immune evasion and recent immunotherapeutic approaches along with their biologic rationale, underscoring the need for integrated therapeutic strategies that both target immunosuppressive elements and enhance immune activation.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"36 1","pages":""},"PeriodicalIF":36.2,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Molecular Subtypes of Neuroendocrine Carcinoma: From Chaos to Consensus. 神经内分泌癌的分子亚型：从混乱到一致。
IF 36.2 1区 医学
Annual Review of Pathology-Mechanisms of Disease Pub Date : 2025-10-08 DOI: 10.1146/annurev-pathmechdis-042524-023153
Zhanyu Wang,Nan Sun,Jie He,Esther Redin,Charles M Rudin
{"title":"Molecular Subtypes of Neuroendocrine Carcinoma: From Chaos to Consensus.","authors":"Zhanyu Wang,Nan Sun,Jie He,Esther Redin,Charles M Rudin","doi":"10.1146/annurev-pathmechdis-042524-023153","DOIUrl":"https://doi.org/10.1146/annurev-pathmechdis-042524-023153","url":null,"abstract":"Neuroendocrine carcinomas (NECs) represent a notoriously aggressive family of lethal malignancies arising across diverse anatomical sites. Molecular subtyping based on key transcription factors ASCL1, NEUROD1, POU2F3, and YAP1 has significantly advanced understanding of tumor heterogeneity in small cell lung cancer (SCLC). Beyond SCLC, extrapulmonary NECs demonstrate analogous heterogeneity, similarly governed by these transcriptional determinants. Recent studies have further identified a fifth subtype driven by the lineage-specifying factor HNF4A. This review aims to propose a unified pan-NEC classification framework for consistent molecular subtyping across pulmonary, gastro-entero-pancreatic (GEP), and genitourinary systems. We delineate the distinct lineage hallmarks of the ANHPY subtypes (neuroendocrine, neuronal, GEP-like, tuft-like, and epithelial-mesenchymal transition phenotypes) and explore their connections to defining mechanisms, genetic alterations, clinicopathological features, and therapeutic vulnerabilities. This unified framework serves as a molecular roadmap for precise NEC research and management.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"62 1","pages":""},"PeriodicalIF":36.2,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Role of Chromatin Looping Factors in Leukemia. 染色质环化因子在白血病中的作用。
IF 36.2 1区 医学
Annual Review of Pathology-Mechanisms of Disease Pub Date : 2025-09-15 DOI: 10.1146/annurev-pathmechdis-051222-014420
Shira G Glushakow-Smith,Zuzana Tothova
{"title":"Role of Chromatin Looping Factors in Leukemia.","authors":"Shira G Glushakow-Smith,Zuzana Tothova","doi":"10.1146/annurev-pathmechdis-051222-014420","DOIUrl":"https://doi.org/10.1146/annurev-pathmechdis-051222-014420","url":null,"abstract":"Genomic organization requires an intricate balance between the compact storage of genetic material and the ability to finely tune gene regulation. Chromatin looping achieves this balance by organizing concordantly regulated groups of genes and their regulatory elements into loops while also condensing DNA to fit into the small volume of a nucleus. A number of DNA-binding and associated proteins, including CTCF and cohesin, act as chromatin looping factors that mediate this process. Given the tight association between chromatin looping and gene expression, disordered genomic organization has been linked to disease development, including cancer. Recurrent mutations in chromatin looping factors are common in cancer, in particular blood cancers such as leukemia and myelodysplastic syndromes. In this review, we describe the evolution of our understanding of the chromatin looping process in healthy and malignant hematopoiesis and discuss the therapeutic potential of targeting chromatin looping factors in leukemia.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"72 1","pages":""},"PeriodicalIF":36.2,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145068435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Exploring the Complex Pathophysiology of Necrotizing Enterocolitis in Preterm Neonates. 探讨早产儿坏死性小肠结肠炎的复杂病理生理学。
IF 36.2 1区 医学
Annual Review of Pathology-Mechanisms of Disease Pub Date : 2025-09-15 DOI: 10.1146/annurev-pathmechdis-070224-014223
Bo Li,Mina Yeganeh,Dorothy Lee,Sinobol Chusilp,Felicia Balsamo,Niloofar Ganji,Chen-Yi Wang,Andrea Zito,George Biouss,Agostino Pierro
{"title":"Exploring the Complex Pathophysiology of Necrotizing Enterocolitis in Preterm Neonates.","authors":"Bo Li,Mina Yeganeh,Dorothy Lee,Sinobol Chusilp,Felicia Balsamo,Niloofar Ganji,Chen-Yi Wang,Andrea Zito,George Biouss,Agostino Pierro","doi":"10.1146/annurev-pathmechdis-070224-014223","DOIUrl":"https://doi.org/10.1146/annurev-pathmechdis-070224-014223","url":null,"abstract":"Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in preterm neonates, with a mortality rate of 30-50% in advanced cases. Despite decades of research, its multifactorial pathophysiology remains incompletely understood. This review summarizes recent advances in NEC research and proposes an integrative theoretical framework for its pathogenesis. We examine key contributing factors, including intestinal vascular development, mucosal immunity, intestinal regeneration, the enteric nervous system, and the gut microbiome, highlighting how prematurity disrupts these processes and predisposes neonates to NEC. Furthermore, we propose a sequential model of NEC pathogenesis, hypothesizing that impaired intestinal microcirculation in preterm neonates compromises blood flow in response to enteral feeding, leading to localized ischemia. This initiates epithelial barrier dysfunction, exacerbates inflammatory responses, impairs intestinal regeneration, and disrupts enteric nervous system function, collectively driving NEC progression. By integrating experimental and clinical findings, we provide a comprehensive perspective on NEC initiation in preterm neonates and identify potential avenues for future research and therapeutic interventions.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"13 1","pages":""},"PeriodicalIF":36.2,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145068438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Clonal Hematopoiesis in Nonmalignant Disease: Functional Consequences of Mutated Immune Cells by Clonal Hematopoiesis in the Diseased Tissue. 非恶性疾病中的克隆造血：病变组织中克隆造血导致免疫细胞突变的功能后果。
IF 36.2 1区 医学
Annual Review of Pathology-Mechanisms of Disease Pub Date : 2025-09-10 DOI: 10.1146/annurev-pathmechdis-111523-023442
Youngil Koh,Isak W Tengesdal,Siddhartha Jaiswal
{"title":"Clonal Hematopoiesis in Nonmalignant Disease: Functional Consequences of Mutated Immune Cells by Clonal Hematopoiesis in the Diseased Tissue.","authors":"Youngil Koh,Isak W Tengesdal,Siddhartha Jaiswal","doi":"10.1146/annurev-pathmechdis-111523-023442","DOIUrl":"https://doi.org/10.1146/annurev-pathmechdis-111523-023442","url":null,"abstract":"Clonal hematopoiesis, originally identified as a precursor to hematologic malignancies, has emerged as a significant factor in various nonmalignant diseases. Recent research highlights how somatic mutations in hematopoietic stem cells lead to the expansion of circulating mutated immune cells that exert profound effects on organ function and disease progression. These mutated clones display altered inflammatory profiles and tissue-specific functional consequences, contributing to various diseases including atherosclerotic cardiovascular disease, osteoporosis, heart failure, and neurodegenerative conditions. Key mutations, particularly in genes regulating epigenetics (TET2, DNMT3A, ASXL1), splicing (SF3B1, U2AF1), and DNA damage repair (TP53, PPM1D), modify immune responses and promote chronic inflammation. Intriguingly, while clonal hematopoiesis exacerbates many inflammatory conditions, it has been linked to a protective effect in Alzheimer's disease, potentially due to enhanced microglial function. Understanding the mechanistic underpinnings of clonal hematopoiesis in nonmalignant disease may inform targeted therapeutic strategies, particularly those aimed at modulating inflammation. This review explores the gene- and organ-specific roles of clonal hematopoiesis, highlighting its implications for disease pathogenesis and potential interventions.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"45 1","pages":""},"PeriodicalIF":36.2,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145031789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Fibroblast Modulation of Stem Cell Lineage Infidelity and Metaplasia in Tissue Fibrosis 成纤维细胞对组织纤维化中干细胞谱系不忠和化生的调节
IF 36.2 1区 医学
Annual Review of Pathology-Mechanisms of Disease Pub Date : 2025-08-21 DOI: 10.1146/annurev-pathmechdis-042624-111827
Tsukasa Kadota, Tien Peng
{"title":"Fibroblast Modulation of Stem Cell Lineage Infidelity and Metaplasia in Tissue Fibrosis","authors":"Tsukasa Kadota, Tien Peng","doi":"10.1146/annurev-pathmechdis-042624-111827","DOIUrl":"https://doi.org/10.1146/annurev-pathmechdis-042624-111827","url":null,"abstract":"Epithelial stem cells are segregated on the basis of region-specific identities during homeostasis. However, tissue perturbations can induce remarkable plasticity in stem cells to adopt lineage identities outside their anatomical compartments. This phenomenon has been termed lineage infidelity or metaplasia depending on the tissue, and the stem cell trajectory can determine regenerative outcomes relevant to many diseases, including fibrosis. While many studies have shed light on stem-cell intrinsic mechanisms that govern their ability to switch identities, much less is known about microenvironmental factors that alert stem cells and modify their lineage decisions. Fibroblasts are structural cells that provide the necessary scaffolding for stem cells in their native niche, but fibroblasts also sense external changes to the tissue environment to drive the tissue response. In this review, we explore the role of fibroblasts as a critical orchestrator of lineage plasticity that blurs compartmental identities to initiate proper repair or disease.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"19 1","pages":""},"PeriodicalIF":36.2,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144898420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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